SUMMARY Using the hydrogen clearance technique, local cerebral blood flow (LCBF) in 22 dogs was estimated at 6 parietal sites prior to and following 5 min of total global ischemia. Ischemia was immediately followed by an initial reactive hyperemia during which the electrocorticogram (ECoG) usually began to recover, and within the first 30 min, most of the LCBPs decreased to subnormal values. This onset of bypoperfusion was accompanied by a concomitant decrease in ECoG activity. Two animals that maintained normal local perfusion after the initial hyperemia recovered ECoG activity quickly. These results suggest that the subsequent poor reperfusion was caused by an increased microvascular resistance rather than by blood aggregates, increased blood viscosity, or a variety of other mechanisms which have been proposed. Increased vascular tonus was, at least, partly responsible for the increased vascular resistance. This report supports the hypothesis that impaired reperfusion (which occurs some time after an initial hyperemia) may be responsible for ultimate neuronal death, rather than the period of global ischemic hypoxia per se.
SUMMARY Following 5 minutes of global ischemia, local cerebral blood flow (LCBF) was shown to have an initial reactive hyperemia that was followed, within the first hour, by persistent hypoperfusion (Part I). Intracranial pressure (ICP) was never elevated during the period of poor reperfusion. These experiments attempted to reverse the state of subnormal LCBF by inducing hypercarbia or hypocarbia or maintaining normocarbia. Although hypocarbia did increase LCBF at several electrode sites, neither the intracerebral steal syndrome nor the "squeeze" syndrome are a dominant consequence of hypercarbia in this model of global ischemia. Hypercarbia was consistently more effective in elevating LCBFs and in recovery of the electrocorticogram. It appears that, in the absence of raised ICP, hypercarbia may be preferred to normal or low Paco 2 . Even though hypercarbia was superior to normocarbia or hypocarbia, hypercarbia was not a completely satisfactory regimen for reversing the state of poor reperfusion.
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